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Y2 NnD > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

When does LOS relax in the process of swallowing

A

As soon as swallowing is initiated

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2
Q

What is the course of the left recurrent laryngeal nerve

A

It goes around the aortic arch

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3
Q

Two main groups of dysphagia and how do they differ

A

Oropharyngeal => vast majority is neurological, food can’t go into oesophagus
Oesophagal=> food is stuck in oesophagus (typically report something stuck at back of sternum)
eg. motility disorders or mechanical obstruction like cancer??

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4
Q

What does cough in GORD indicate

A

Acid goes as far as back of throat and gets into respiratory system ⇒ Hoarse voice, cough and bronchospasm

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5
Q

What does weight loss in upper GI symptoms suggest

A

Cancer or severe motility syndroms

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6
Q

What is barium swallow more commonly used for and what does it show

A

Monitor motility of oesophagus, diagnose presence of hiatus hernia

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7
Q

First line investigation for cancer suspicion

A

Urgent upper GI endocsopy

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8
Q

What should be used for staging of oesophageal cancer and what is good to see spread of tumour

A

Endoscopic ultraspund, CT (thorax and abdomen) or CT -PET

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9
Q

What is the narrowing of the oesophagus called

A

Stricture

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10
Q

Causes of benign strictures

A

GORD, Barret’s more common causes
- Extrinsic compression from tumours in the mediastinum or lung
- Post-radiotherapy ⇒ Mainly for malignant disease
- Anastomotic ( following surgery / oesophagectomy)
- Corrosive ( accidental or suicidal ingestion) ⇒ can leas to extensive, complex strictures and may end up with oesophagectomy

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11
Q

Main treatment of strcitures

A
  • Proton pump inhibitors (e.g. omeprazole) ⇒ If not severe, especially if it is mainly due to significant inflammation
  • Dilatation (best treatment)
    • Push dilators
      • Celestin gradual dilators up to 18mm ⇒ Inserted with a guard wire passed across the stricture, and gradually dilate
  • Savary-Gillard polyvinyl dilators ⇒ balloon
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12
Q

What is one main risk factor of GORD and when do symptoms get more obvious

A

Obesity, bending over

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13
Q

Two main kind of reflux and how they vary

A
  • Reflux with Transient lower oesophageal relaxations
    • More common
    • Daytime reflux
    • Small or no Hiatus hernia (very rare)
    • Often no oesophagitis ⇒ As acid usually cleared by oesophagus quite fast
  • Reflux with low lower oesophageal sphincter pressures
    • Less common (20%)
    • Nocturnal reflux
    • Often large hiatus hernia
    • More severe oesophagitis ⇒ Due to presence of large amounts of acid in oesophagus over long periods
    • Barrett’s ⇒ Chronic exposure to acid
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14
Q

Possible history of GORD

A
  • Weight gain ⇒ LOS infiltrated by fat so not as effective
  • Lifestyle and diet- citrus food, fizzy drinks, chocolate, spicy foods, tomato sauce
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15
Q

What are the possible signs of hiatus hernia

A
  • Regurgitation of food and fluid ⇒ Sphincter is really loose, not that common
    • Probable Hiatus Hernia ⇒ Sphincter almost disappears , more prone to acid reflux and regurgitation
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16
Q

Possible treatment for GORD and Barret’s
Mechanical, surgical, lifestyle

A

Surveillance vs. Ablation using balloon to kill cells for Barrett’s ( so it doesn’t become malignant)
GORD:
Long term Tx with PPIs- main measure
Lifestyle- smoking, alcohol, diet, weight reduction
Surgical - fundoplication to tighten sphincter in younger ppl

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17
Q

What does equal dysphagia to liquid and solids in younger ppl suggest

A

Achalasia

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18
Q

What is the cause of achalasia

A

Infiltration of esoinophils - failure of LOS relaxation and absence of peristalsis.
Degenerative lesion of myenteric plexus which innervates oesophagus

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19
Q

Investigation and diagnosis of achalasia

A

UGE, but may be normal, Barium swallow for diagnosis, dilates oesophagus with hypertonic LOS
Manometry to confirm

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20
Q

Treatment for achalasia

A

Botox for older patients to paralyse LOS
Endoscopic pneumatic dilatation for young, middle age- to dilate and disrupt the LOS
Surgical Myotomy
- cut open LOS to open lower end of oesophagus, but longer lasting effect
POEM- small incision in the wall of the oesophageus, cut LOS and clip the incision

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21
Q

What is a likely cause of food bolus obstruction with dysphagia

A

Eosinophilic esophagitis - common in younger ppl also

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22
Q

History of eosinophilic oesophagitis

A

Atopy

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23
Q

Investigations and diagnosis of eosinophilic oesophagitis

A

Endoscopy for furrows , rings, exudates and strictures. But need biopsy for diagnosis - > 15 esosinophils then diagnosis is secure

24
Q

Treatment for Esoinophilic oesophagitis

A

Diet - elimination of allergic stuff
Drugs - PPI for acid elimination
Topical steroids like orodispersible budesonide eg. Jorvesa
Can use dilatation for strictures

25
Q

What are the fundic glands in the stomach

A

Oxyntic/ parietal cells which produce HCL and IF- needed for Vit B12 absorption
Chief cells- pepsinogen, renin and lipase
Neck cells that secrete mucus
Enteroendoctine cells - gastrin, CCK, secretin, serotonin, glucagon

26
Q

What are the main arteries in the coeliac axis that supplies duodenum

A

supraduodenal and gastroduodenal arteries.

27
Q

Where can a peptic ulcer disease be found

A

Oesophagus, a/o stomach a/o duodenum

28
Q

Diff btw ulcer and erosion

A

Ulcer will penetrate the muscularis mucosae and may therefore meet vessels . Erosion is just superficial penetration of mucosa

29
Q

Presentation of dyspepsia caused by helicobacter pylori

A
  • Abdominal pains increasing for months
  • Vomiting hours after eating
  • Epigastric pains
  • Loss of appetite
  • Weight loss
  • Intermittently tarry stool⇒ Chronic blood loss from upper GI (bleeding)
30
Q

How does h. pylori cause ulcers

A

Can alter balance between hyperacidity and mucosal defence in lining of stomach, leading to ulceration

31
Q

What investigations should be used for H. Pylori (non-invasive)

A

C13 Breath test - radiolabelled Co2 will be exhaled . May also used stool antigen test which is reliable and done in primary care.

32
Q

What can biopsy do for H. pylori infection

A

Can show inflammation, histology may be done using biopsies, can do CLO test. Petri dish with pH indicator, biopsy will turn red if positive

33
Q

How to treat H.pylori

A

triple therapy- PPI (lansoprazole) , 2 antibiotics like Clarithromycin and Metronidazole ( amoxicillin for second line)

34
Q

Main causes of dyspepsia

A

Peptic ulcer disease, GORD, functional

35
Q

What factors affect the risk of peptic ulcer disease

A

Smoking cause increased risk, delayed healing

36
Q

What is Zollinger Ellison syndrome

A

Excess gastrin – gastrinoma, can cause peptic ulcer disease

37
Q

What are the symptoms of peptic ulcer perforation

A
  • Peritonitis, shock
  • Sudden severe pain
  • Shoulder tip pain
  • Air under the diaphragm (bilateral) as air escapes through the peritoneum and goes up
38
Q

What are the signs of peptic ulcer bleeding in upper GI

A

Haematemesis, Melaena or both may occur

39
Q

Principles of management of upper GI bleeding

A

Assessment of severity, then giving IV crystalloid, colloids or blood, intensive monitoring in crititical cate, early endoscopy, and depending on the case, HP eradication, PPIs and and other ways to stop bleeding eg. adrenaline, heat, hemospray, clips and lastly surgery

40
Q

What are the two important arteries at risk of bleeding- what can be done if it bleeds?

A

supraduodenal and gastroduodenal- put catheters there

41
Q

Functional dyspepsia - what are the two main syndromes

A

Post-prandial distress syndrome
- Fullness and satiety but no pain ⇒ May accommodate food in stomach more much longer
- Discoordination in stomach
- Gastric dysmotility or abnormal accommodation.

Epigastric pain syndrome - pain and burning => visceral hypersensitivity

42
Q

Initial investigations for functional dyspepsia

A
  • Stool or breath test for H. Pylori ⇒ Peptic Ulcer Disease
  • Upper GI endoscopy ⇒ Recommended to exclude organic disease
    • Exclude systemic or metabolic disease (eg diabetes
  • If both normal, most likely diagnosis is FD
43
Q

How to differentiate between peptic ulcer disease and functional dyspepsia

A

Tends to have more obvious symptoms like vomitting, stopping eating, waking up in middle of the night.
If from Eastern Europe, may be more likely

44
Q

How to differentiate functional dyspepsia and GORD

A

More likely to have symptoms like Heartburn, acid regurgitation and waterbrash

45
Q

What is the Rome IV criteria for functional dyspepsia

A

Criteria fulfilled for the last 3 months with symptom onset at least 6 months before diagnosis

  • Bothersome postprandial fullness
  • Bothersome early satiety
  • Bothersome epigastric pain
  • Bothersome epigastric burning

And no evidence of structural disease at upper endoscopy

46
Q

Possible causes of functional dyspepsia

A

Low-grade immune activation and dysregulation of gut-brain axis, impaired mucosal integrity, gd motor and sensory dysfunction

47
Q

Factors that may affect occurence of FD

A

Acute infection, genetic predisposition, psychiatric disorders, abise

48
Q

Treatment for FD

A

PPIs and H2 antagonists to reduce acids, Metoclopramide for fullness and sickness, SSRI tricylcis for hypersenstitivity

49
Q

Where does left gastric vein drain

A

Blood from lesser curvature of stomach, branches from fundus of stomach

50
Q

What is the presentation of acute pancreatitis

A

Acute epigastric back pain, RUQ or LUQ, pain can be colicky or continuous, may have N and V, fever or tachycardia, jaundice, Grey Turner’s or Cullen’s sign

51
Q

How to diagnose for acute pancreatitis

A
  • High Amylase > x 3 normal or Lipase ( longer ½ life)
    ( NO prognostic significance)
    • Pancreas might be digested by amylase, causing holes and pseudo cyst, necrotic areas
52
Q

Main causes of acute pancreatitis

A

Small gallstone stuck in ampulla, alchohol

53
Q

Less common causes of acute pancreatitis

A

Post ERCP pancreatitis (3-8% of ERCPs) ⇒ to remove stones from common bile duct
- Metabolic ⇒ Hyperlipidaemia - High TG, Hypercalcaemia
- Drug induced ⇒ Azathioprine, steroids
- Viral
- Pancreatic Ca
- Idiopathic
- Autoimmune

54
Q

How to get differential diagnosis for acute pancreatitis

A

Use CT scan

55
Q

Common complications of acute pancreatitis

A

Hypocalcaemia and hypoxia , paralytic ileus not uncommon, may have hypovolaemia in severe cases , RF, DIC ,effusion

56
Q

Main management plan of Acute pancreatitis

A

Supportive measures- decompress ducts if have gallstones, IV and antibitoics if septic in certain cases. May have ERCP. Need to drain large pseudocysts`

57
Q

How does non-variceal bleed occur

A

Ulcers can invade the artery and cause bleeding

Y2 NnD (10 decks)

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